Investigation of fatal congenital Zika cases show injury to spinal cord caused by virus

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Report gives evidence that neurological impacts of Zika go beyond effects on brain development

By the time pediatric pathologists explored the cases reported in the August Clinical Infectious Diseases of two infants, both congenitally infected with Zika, both of whom had died shortly after birth, knowledge of the damage the virus could do to the brains of fetuses had gone well beyond the most apparent impact of microcephaly. The virus, found in the brains of babies and fetuses disrupted brain cell development, killed brain cells, and led to atrophying of nerves essential to seeing and hearing, as well as thinning of the cerebral cortex, the outermost layer of the brain’s nerve cell tissue, critical to perception, language, memory and awareness. In addition, doctors and researchers had noted infants affected by the virus sometimes had limited movement of their arms and legs.

Post-mortem examinations of the two newborn babies, according to the report, add new understanding of the impacts of Zika to infants and fetuses of mothers infected during pregnancy, providing evidence that the virus also can cause severe damage to the spinal cord. Both infants were born slightly prematurely to women who had suffered from rash and fever during the first trimester of pregnancy, one weighing less than three pounds, the other slightly less than four pounds. Both had skull and facial deformities. One died 18 minutes after birth, and the other seven hours after being delivered by Cesarean section. Examination of each found extensive brain damage, as well as evidence of the virus in their brain tissue. In addition, for the first time, according to the report, pathologists also identified evidence of the virus in infants’ spinal cords, as well as extensive damage to spinal cord structure and cells. In neither infant, the authors note, was the virus found in other organs including their heart, lungs, kidneys, or livers.

The findings are significant, the authors, led by Fernando S. Ramalho of the University of São Paulo, write, because damage done by the virus to the spinal cord must now also be considered to explain motor deficits in children affected by the virus, and should lead to investigation among larger numbers of congenitally infected children.

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